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ANG — SMAD3

Text-mined interactions from Literome

Wang et al., Circ Res 2006 (Arteriosclerosis...) : Finally, activation of Smad3 but not Smad2 was a key and necessary mechanism of Ang II-induced vascular fibrosis because Ang II induced Smad3/4 promoter activities and collagen matrix expression was abolished in VSMCs null for Smad3 but not Smad2
Lee et al., Nephrol Dial Transplant 2007 (Diabetes Mellitus, Experimental...) : COMP-Ang1 also reduced renal tissue levels of transforming growth factor-beta1 ( TGF-beta1 ), alpha-smooth muscle actin, fibronectin, as well as Smad 2/3 expression, but increased Smad 7 expression
Yang et al., J Pathol 2010 (Kidney Diseases) : In conclusion, Ang II activates Smad signalling to induce EMT, which is mediated by a loss of Smad7 through the AT1-Smurf2 dependent ubiquitin degradation pathway